In a study published this week in Immunity, scientists at NYU Langone Medical Center have discovered that in addition to white blood cells, other cells such as epithelial and endothelial cells also respond to interferon gamma and also protect mice from uncontrolled tuberculosis infection. This new pathway could lead to the developments of treatments that could limit or prevent tissue damage resulting from inflammation.
“Through research on tuberculosis, we discovered a new way that the immune system response is controlled,” said lead author Joel Ernst, MD, director of the Division of Infectious Diseases and the Jeffrey Bergstein Professor of Medicine at NYU Langone Medical Center. “Further study may reveal treatments that could be useful in control of inflammation and tissue damage in certain infections and autoimmune diseases.”
In this study, researchers looked at interferon gamma responses in epithelial and endothelial cells to control tuberculosis in mice. Cells such as epithelial andendothelial cells were found to respond to interferon gamma by producing an enzyme, indolelamine-2-3-dioxygenase (IDO), that converts the amino acid tryptophan to products called kynurenines. These kynurenines inhibit the production of Th17 cells, the lymphocytes that contribute to tissue-damaging inflammation.
The study’s co-author is Ludovic Desvignes, PhD, of the Department of Microbiology at NYU Langone Medical Center. The research was funded by grants from the National Institute of Allergy and Infectious Diseases of the National Institutes of Health in Bethesda, Maryland.
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